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At least 19 recordsLinked to original sources
PubMed1975

[Idiopathic necrosis in the marrow of the distal femur. A contribution to aseptic necrosis of the bone (author's transl)].

Symmetrical aseptic necrosis in the marrow of the distal femur was systematically examined in 4 autopsies. According to formal analysis, the self reliant process, with a tendency toward relapse begins with two forms of destruction of the medullary fatty tissue. The consequences are fundamentally the same as those present after necrosis of the extra-medullary fatty tissue; there are only modifications caused location. These modifications include the regular calcification of non-liquifying by fatty-tissue necrosis that fibroses in a net-like manner, and of subsequent bone formation. Spongiosis in incorporated secondarily into necrosis. Medullary necrosis are not caused by vascular lesions and differ therefore from infarct-like necrosis of the bone. The etiology of the medullary steatonecrosis, which probably begins dystrophically, cannot be cleared up morphologically, and is unknown up to now. There are no definite indications for a causal relationship with cortico-steroid therapy. This form of necrosis of the marrow is therefore termed "idiopathic".

Adipose Tissue↗
PubMed1979

Cell killing by spleen necrosis virus is correlated with a transient accumulation of spleen necrosis virus DNA.

Spleen necrosis virus productively infects avian and rat cells. The average number of molecules of unintegrated and integrated viral DNA in cells at different times after infection was determined by hybridization and transfection assays. Shortly after infection, there was a transient accumulation of an average of about 150 to 200 molecules of unintegrated linear spleen necrosis virus DNA per chicken, turkey, or pheasant cell. No such accumulation was seen in infected rat cells. Soon after infection there was in chicken cells, but not inturkey, pheasant, or rat cells, also a transient integration of an average of 35 copies of viral DNA per cell. By 10 days after infection, the majority of this integrated viral DNA was lost from the population of infected chicken cells. At the same time, the majority of the unintegrated viral DNA was also lost from infected chicken, turkey, and pheasant cells. The transient cytopathic effect seen in these infected cells also occurred at this time. Late after infection about five copies of apparently nondefective spleen necrosis proviruses were stably integrated at multiple sites in chicken, turkey, pheasant, and rat DNA. These results demonstrate a correlation between the transient accumulation of large numbers of spleen necrosis virus DNA molecules and the transient occurrence of cytopathic effects.

Animals↗
PubMed1978

Fat necrosis - a cause of pancreatic parenchymal necrosis?

Acute pancreatic necrosis resulted when oleic acid or olive oil was injected into the pancreatic duct or rats. After injection of droplets of both lipids into the pancreatic interstitial tissue, coagulation-type necrosis of acinar tissue developed adjacent to these droplets. Mono-olein or paraffin oil caused no histological alterations of acinar cells. It is concluded that (1) the deleterious effect of olive oil on the pancreas is mediated through fatty acids released by pancreatic lipase, and (2) fatty acids split off in fat necrosis of acute pancreatitis may damage adjacent pancreatic acinar tissue.

Adipose Tissue↗
PubMed1979

Bone marrow necrosis and extramedullary myeloid tumour necrosis in aggressive chronic myeloid leukaemia.

A patient with chronic myeloid leukaemia who developed widespread bone marrow necrosis associated wtih evolution of a new cell clone and with aggressive behaviour of the myeloid tumour in extramedullary sites is described. Cell necrosis in extramedullary tumours was also present; the sharp demarcation between zones of necrotic cells and intact cells and the histological evidence of vascular invasion by tumour cells suggest a vascular basis for cell necrosis.

Bone Marrow Diseases↗
PubMed1976

Skeletal muscle necrosis following membrane-active drugs plus serotonin.

Administration of imipramine plus serotonin (5-HT) to rats has been proposed as an animal model of Duchenne muscular dystrophy. We studied the skeletal muscle necrosis produced in male rats given 5-HT after pretreatment with imipramine, other tricyclic antidepressants, or antihistamines, which like the tricyclic antidepressants, can block neuronal reuptake of 5-HT. Following one of these agents plus 5-HT, 20 mg/kg subcutaneously (s.c.), necrosis was more severe in the soleus muscle than the quadriceps. There was no significant difference in the incidence of necrosis in the soleus and quadriceps muscles following one of these agents plus 5-HT, 100 mg/kg, intraperitoneally (i.p.). After one of these agents plus 5-HT i.p., but not 5-HT s.c., extensive necrosis was significantly more frequent and severe in the quadriceps muscle than after 5-HT s.c. Chlorpheniramine (CP) plus 5-HT, 2.5 mg/kg intravenously, produced less muscle necrosis than CP plus 5-HT s.c. or i.p. The necrosis produced by CP plus 5-HT s.c. was comparable ipsilateral and contralateral to the injection site. The necrosis following CP plus 5-HT i.p. was maximal at 24 hr and remained fairly constant until 5 days. Regeneration was prominent by 7 days. The muscle necrosis produced by CP plus 5-HT is blocked by some 5-HT blockers, e.g., methiotepin and methysergide. It is also partially blocked by denervation. The capacity of tricyclic antidepressants and antihistamines to block neuronal 5-HT reuptake tended to be negatively correlated with the capacity to potentiate the muscle necrosis they produced with 5-HT, which suggests that blockade of 5-HT uptake is not the mechanism of the pathology produced by the combined treatment. The tricyclic antidepressants and the antihistamines are "membrane stabilizers-labilizers". Other drugs which are "membrane stabilizers-labilizers" such as trihexyphenidyl and procaine also promoted skeletal muscle necrosis when given prior to 5-HT. It is proposed that the effects of imipramine plus 5-HT on skeletal muscle are not due to the blockade of neuronal uptake of 5-HT and subsequent vascular-induced ischemia, but reflect direct toxic effects of these agents on skeletal muscle.

Animals↗
PubMed1979

[Usefulness of creatine phosphokinase isoenzyme, CK-MB, in the diagnosis of myocardial necrosis (author's transl)].

With the objective of evaluating the clinical usefulness of a new immunologic method (Merck-1-Test CK-MB), in the determination of the CK-MB activity, 48 patients admitted to the Coronary Unit for angina pectoris were studied. Samples of blood were gathered upon admission and every 4 hours for 48-72 hours, determining in each one of them the total CPK, SGOT, LDH, and CK-MB; electrocardiograms (ECG) were taken and all possible causes for the increase in the enzymatic activity were recorded. Results were analyzed in order to study the following aspects: in the patients in which an acute myocardial infarction was diagnosed the CK-MB activity was studied, also the relation of CK-MB to the remaining parameters, each parameter's sensitivity and specificity and the relationship of the CK-MB to the prognosis of the patients. The usefulness of CF-MB in the differential diagnosis of myocardial necrosis and variations in the total CKP curve in the clinical course of acute myocardial infarction unrelated to myocardial necrosis were evaluated too. The following conclusions were drawn from the analysis of the data. The immunological method has the advantages of its sensitivity and easily and quickly performance (15 minutes), but it has the disadvantage that it detects CK-BB (elevated in cebrovascular disorders). Twenty-four hours after the onset of symptoms, the negativity of CK-MB does not exclude the diagnosis of a myocardial necrosis. CK-MB is more sensitive than total CPK in diagnosing the extent of the area of necrosis. CK-MB is very specific for myocardial necrosis but less sensitive than other parameters. A positive CK-MB upon the patient's admission confirmed the diagnosis of necrosis in 60 percent of the cases, but in 18 percent error was induced because of false positives. CK-MB permitted confirmations of the diagnosis of myocardial infarction in 33 percent of cases in which there was only a suggestion of necrosis by the ECG. The variation in the curve of total CPK in the course of an acute myocardial infarction is subjected to such a great number of factors intercurrent with time, that caution should be exercised in trying to relate a specific elevation of total CPK to an unsuccessful maneuver or to a possible extension of the area of necrosis.

Adult↗
PubMed1977

Myocardial consequences of coronary artery bypass graft surgery. The paradox of necrosis in areas of revascularization.

Myocardial infarction after coronary artery bypass graft (CABG) surgery has been described clinically in up to 30% of patients but there is little morphologic information about the character and pathogenesis of the myocardial injury. We studied myocardium in the distribution of bypassed and nonbypassed coronary arteries for the presence of contraction band necrosis as compared to coagulation necrosis, in 58 autopsied patients who died less than 1 month after surgery. Operation related necrosis consisting of focal subendocardial contraction band necrosis was present to some degree in 48 (83%) patients. Regional transmural necrosis was present in 22 (38%) patients and was of two types. Contraction band necrosis occurred in 18 patients and was in the distribution of a patent bypassed coronary artery in 15 of them. Coagulation necrosis was found in four patients, and in each was in the distribution of a new graft-releated coronary artery occlusion. The results suggest that coronary artery reflow through widely patent grafts following the period of operative nonperfusion, rather than graft or intrinsic coronary artery occlusion, accounts for the majority of operation-related myocardial "infarcts" associated with CABG surgery. Thus, prevention of intraoperative myocardial injury must also focus on characteristics of the phase of myocardial reperfusion.

Adult↗
PubMed1979

[Necrosis in cases of slipped upper femoral epiphysis and its consequences (author's transl)].

The author demonstrates the development and treatment of 6 cases of necrosis of the slipped upper femoral epiphysis. In cases of gradual dislocation, the blood supply of the epiphysis remains normal at all stages. Necrosis does not occur spontaneously. In cases of sudden or so-called "traumatic" separation, the supply of blood to the epiphysis is often disturbed, and necrosis may occur spontaneously. Slight disturbance of the blood supply to the epiphysis may be only temporary and complete recovery may take place. Severe damage, however, leads to necrosis. Operative measures to treat the necrosis may lead to an improvement, but complete restoration of necrosis is not possible--as the examples in the article show. Osteoarthritis will follow at an early age in these cases. Thus, to avoid necrosis in cases of sudden dislocation of the epiphysis therapy must be carried out very gently. Closed or operative reduction should not be performed immediately after the slippage. The deformity should be corrected at a later stage.

Adolescent↗
PubMed1978

Experimental renal papillary necrosis in the rat: the selective vulnerability of medullary structures to injury.

Acute renal papillary necrosis was produced in rats by the administration of ethyleneimine. Low doses resulted in necrosis of interstitial cells, thin limbs of the loops of Henle and vasa recta, while collecting ducts were spared (subtotal renal papillary necrosis). High doses resulted in necrosis of all elements of the papilla (total renal papillary necrosis). Athough the ranges of the doses that produced these two patterns of necrosis overlapped, it is clear that there is a dose dependent selective vulnerability or renal medullary structures to injury by the toxic agent studied.

Animals↗
PubMed1978

[Studies of lipase-induced fat necrosis in rats (author's transl)].

Disseminated fat necrosis can be produced by intraperitoneal injection of porcine pancreatic lipase. They get detecable by intravital staining with Phosphine 3R about 15 min after injection. The earliest fine structural findings are spotty destruction of the pinocytic invaginations and vesicles, combined with alterations of the cell membrane. Later there is a complete destruction and disintegration of the cytoplasm and its organels as well as the nucleus, whereas the cell membrane partly remains visible. At the same time the central lipid droplet shows cloudy disintegration and clumping as well as cristalline and granular structures. In the beginning the necrosis is limited to single cells. Later the adjacent fat cells also undergo necrosis, even when the applicated lipase has been removed after 30 min. In light microscopic studies fat necrosis are detectable 30 min after the application of lipase. During the first 48 hours they get demarcated by leucocytes. In the following days resorption and organisation take place. Lipolytic drugs facilitate the development of fat necrosis, whereas antilipolytic drugs inhibit it. In starvation the number of fat necrosis rises, after feeding it decreases. In the diurnal rhythm there is a maximum after midnight and a minimum in the early afternoon. The results support the hypothesis that pancreatic lipase only attacks fat cells, which are lipolytically active.

Adipose Tissue↗
PubMed1978

Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs.

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.

Animals↗
PubMed1979

[Early observations of pancreatic ultrastructure during hemorrhagic necrosis in the rat with closed duodenal pouch].

Many problems are still unanswered in the pathogenesis of acute clinical and experimental pancreatic necrosis. A new technique which can be performed in the rat seems a suitable model for reflux pancreatic necrosis without artificial pressure changes in the ductal system. A closed duodenal loop is obtained with ligation proximal and distal to Vater's ampulla and a gastroenteroanastomosis is associated to avoid intestinal obstruction. All the rats die with hemorrhagic pancreatic necrosis in 36 hours. After 12 hours from the operation ductal and acinar lumina are enlarged. In the centroacinar and intercalated duct cells some lysosomes and mitochondria with clear matrix and reduced cristae are detected. Intercellular junctions in ducts and acini have normal morphology. In the basal cytoplasm of acinar cells some prominent autophagic vacuoles are detectable. After 24 hours in the acinar cells autophagic vacuoles are greatly increased and basal cytoplasmic degeneration often occurs, with plasmalemma and basal lamina interruptions. Intercellular junctions are apparently unaffected until cell necrosis sets in. In blood capillaries endothelial cells are swollen, fibrin thrombosis, hemorrhage and leucocyte infiltration are often detectable. As lysosomal activity occurs also in different kinds of experimental pancreatic necrosis, it could be a common pathogenetic factor, responsible for hydrolytic enzyme activation and for vascular damage in the early stages of hemorrhagic pancreatic necrosis.

Animals↗
PubMed1979

Acute retinal necrosis.

Three cases of acute retinal necrosis are presented. Acute retinal necrosis is an unusual syndrome which is the result of severe contusion to the globe. It is characterized by large irregular retinal holes with pieces of necrotic retina in the adjacent vitreous, retinal edema and hemorrhage surrounding the holes, underlying choroidal disruption, and vitreous hemorrhage. The incidence of acute retinal necrosis is difficult to determine but it does not appear to be common entity. Although acute retinal necrosis may be associated with a retinal detachment, other retinal breaks are usually responsible for the detachment. The necrosis results from the direct force of the injury striking the globe although a contrecoup mechanism may explain cases of nasal necrosis. Treatment is necessary for associated retinal detachments and acute lesions but may not be necessary if adequate fibrosis is present when the lesion is first seen.

Acute Disease↗
PubMed1977

Bone necrosis and urinary hydroxyproline excretion in rabbits.

1. Aseptic necrosis of bone is a serious chronic complication of deep-sea diving and compressed-air work. 2. The changes to the bone which occur in this condition take time to develop to the stage where they cause the radiographic signs of bone necrosis, and consequently there is a delay of some months between the causal incident and the first diagnosis by radiography. 3. As a possible method for the earlier detection of bone necrosis the 24 h urinary excretion of hydroxyproline was measured over a period before and after experimental production of bone necrosis in rabbits by the intra-arterial injection of glass microspheres. 4. Total hydroxyproline excretion rose significantly within a few days of the injection in those rabbits in which there was later shown to be historical evidence of bone necrosis. This rise occurred long before there was any radiographic changes. 5. It is suggested that measurements of urinary hydroxyproline might be used to give an early indication of bone necrosis in man.

Animals↗